Intracellular free calcium accumulation in ferret vascular smooth muscle during crystalloid and blood cardioplegic infusions

Objective: The effects of magnesium- and potassium-based crystalloid and blood-containing cardioplegic solutions on coronary smooth muscle intracellular free calcium ([Ca 2+] i) accumulation and microvascular contractile function were examined. Methods: Isolated ferret hearts were subjected to hyper...

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Published in:The Journal of thoracic and cardiovascular surgery 1999-07, Vol.118 (1), p.163-172
Main Authors: Tofukuji, Motohisa, Matsuda, Naruto, Dessy, Chantal, Morgan, Kathleen G., Sellke, Frank W.
Format: Article
Language:English
Subjects:
Anesthesia
Anesthesia depending on type of surgery
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Biological and medical sciences
Calcium - analysis
Cardioplegic Solutions - chemistry
Cardioplegic Solutions - pharmacology
Coronary Circulation - drug effects
Coronary Vessels - drug effects
Disease Models, Animal
Drug Evaluation, Preclinical
Ferrets
In Vitro Techniques
Intracellular Fluid - chemistry
Isotonic Solutions
Magnesium - pharmacology
Male
Medical sciences
Microcirculation - drug effects
Muscle, Smooth, Vascular - drug effects
Plasma Substitutes - pharmacology
Potassium - pharmacology
Thoracic and cardiovascular surgery. Cardiopulmonary bypass
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Summary:Objective: The effects of magnesium- and potassium-based crystalloid and blood-containing cardioplegic solutions on coronary smooth muscle intracellular free calcium ([Ca 2+] i) accumulation and microvascular contractile function were examined. Methods: Isolated ferret hearts were subjected to hyperkalemic (25 mmol/L K +) blood cardioplegic infusion, hypermagnesemic (25 mmol/L Mg 2+, K +-free) crystalloid cardioplegic infusion, or hyperkalemic crystalloid cardioplegic infusion for 1 hour. Coronary arterioles were isolated, cannulated, and loaded with fura 2. Reactivity and [Ca 2+] i were assessed with videomicroscopy. [Ca 2+] i was measured at baseline and after application of 50 mmol/L KCl. In addition, [Ca 2+] i and vascular contraction were measured during exposure to Mg 2+ and K + cardioplegic solution at both 4°C and 37°C. Results: From a baseline [Ca 2+] i of 177 ± 52 nmol/L, K + cardioplegic infusion (302 ± 80 nmol/L potassium) markedly increased [Ca 2+] i, whereas blood cardioplegic infusion (214 ± 53 nmol/L) and Mg 2+ cardioplegic infusion (180 ± 42 nmol/L) did not alter [Ca 2+] i. Although a difference between groups in percentage contraction after application of 50 mmol/L KCl was not observed, [Ca 2+] i increased significantly more in vessels in the control group (764 ± 327 nmol/L) and the K + crystalloid cardioplegic infusion group (698 ± 215 nmol/L) than in vessels in the blood cardioplegic infusion group (402 ± 45 nmol/L) and the Mg 2+ cardioplegic infusion group (389 ± 80 nmol/L). Mg 2+ cardioplegic solution induced no microvascular contraction at either 4°C or 37°C, nor was an increase in [Ca 2+] i observed. K + cardioplegic solution induced microvascular contraction at 37°C but not at 4°C; it increased [Ca 2+] i at both 4°C and 37°C. Conclusion: An Mg 2+-based cardioplegic solution, or appropriate Mg 2+ or blood supplementation of a K + crystalloid cardioplegic solution, may decrease the accumulation of [Ca 2+] i in the vascular smooth muscle during ischemic arrest. (J Thorac Cardiovasc Surg 1999;118:163-72)
ISSN:0022-5223
1097-685X
DOI:10.1016/S0022-5223(99)70155-8